M2 Macrophage Suppression assay as shuttle session to test your compounds in a cost-saving way

Take advantage of our upcoming in vitro shuttle session scheduled in early July on our validated M2 macrophage suppression assay, to assess novel immunotherapeutics in time and cost-effective manner.

Our M2 suppression assay, based on i) the co-culture of monocyte-derived M2 macrophages and activated T cells and ii) the quantification of IFNg levels as surrogate of T cell activation, is specifically designed to evaluate candidate compounds for their ability to repolarize / switch M2 macrophages and/or to antagonize M2-mediated T cell suppression.
 
To take place on this shuttle, registration is now open - contact us to plan your study(ies)!

Contact us to test your compoud - seating is limited

M2 macrophages are known to display a IL6low IL10high profile, a phenotype known to be underpinned by ‘’overactivated’’ signaling pathways in these cells, such as JAK/STAT and SMAD/p38 MAPK, and to be therefore involved in their T cell response suppression function.

M2 macrophages are known to display a IL6low IL10high profile, a phenotype known to be underpinned by ‘’overactivated’’  signaling pathways in these cells, such as JAK/STAT and SMAD/p38 MAPK, and to be therefore involved in their T cell response suppression function.
M2 macrophage phenotype and its mediated T cell response immunosuppression are reversed by molecular pathway modulators and immune checkpoint inhibitors. (A) HTRF-based quantification of IL6 and IL10 levels released in the supernatants of M2 macrophages, either untreated  or treated with the p38 MAPK inhibitor during their polarization. (B) HTRF-based quantification of IFNγ levels released in the supernatants of activated PBMC/M2 co-cultures performed in the absence and presence of atezolizumab, and in the supernatants of co-cultures of activated PBMC with M2 macrophages that underwent treatment with a p38 MAPK inhibitor during their polarization.

Addition of a p38 MAPK inhibitor during the M2 polarization process is shown to be capable of repolarizing/switching M2 phenotype by reverting, at least partially but dose-dependently, the IL6low IL10high profile (A).

In the co-culture immunosuppression assay with PBMCs (B), M2 macrophages exhibit a strong suppression of T cell activity shown through released IFNg level decrease. M2 suppression function is known to be exerted via multiple mechanisms including PD1/PDL1 axis engagement or pathway modulation, among other ways. Interestingly, co-cultures of activated PBMC with M2 macrophages that underwent treatment with a p38 MAPK inhibitor during their polarization result, at least partially, in a dose-dependent reversal of the T cell activation suppression compared to untreated PBMC/M2 co-cultures. Atezolizumab treatment of co-cultures is also shown to completely and dose-dependently relieve the immunosuppressive M2 function on T cell response, with a reversal of the M2 IFNg release profile.

For more information also visit M2 Macrophage Suppression Assay webpage, or contact us!